Preliminary reports indicate that lithium therapy is effective in selected cases of alcoholism by reducing recidivism and "craving" for alcohol. Other reports indicate that Li ion may cause a lessening of intoxication and milder withdrawal during and after experimental chronic drinking. Since these have been empirical clinical observations it is proposed that experimental studies are needed to establish a rational basis for this activity of Li ion. The probable hypothetical mechanism selected for study is that Li ion may interact with the metabolism of biogenic amine neurotransmitters which has been disturbed by chronic alcohol and produce a corrective shift. Studies in this laboratory have shown that chronic alcohol administration produces an acceleration of nonrepinephrine release and turnover; actions which are similar to the acute effects of acetaldehyde but not ethanol. Since the separate action of chronic Li ion administration on biogenic amine function appears to be a slowing of turnover and/or reduced release of the neurotransmitter, it is proposed to study the effects of Li ion on alcohol-induced changes in biogenic amine function. Rats will be studied for the rate of turnover of H3-norepinephrine, dopamine and serotonin and correlative behavioral tests after chronic intake of Li ion and alcohol using a nutritionally complete liquid diet containing these drugs. It is anticipated that the study will provide a rational basis for the actions of Li ion on alcoholism.